1. Anti-infection Apoptosis Protein Tyrosine Kinase/RTK MAPK/ERK Pathway Stem Cell/Wnt PI3K/Akt/mTOR Cell Cycle/DNA Damage Epigenetics
  2. HIV Apoptosis Caspase VEGFR ERK PI3K Akt mTOR PARP
  3. 1,3,5-Tricaffeoylquinic acid

1,3,5-Tricaffeoylquinic acid acts as an angiogenesis inhibitor and apoptosis inducer, and exhibits anti-HIV activity. 1,3,5-Tricaffeoylquinic acid inhibits the phosphorylation of VEGFR2, ERK, PI3K, Akt and mTOR in the angiogenesis signaling pathway. 1,3,5-Tricaffeoylquinic acid regulates apoptosis-related proteins, upregulates the levels of activated caspase-8, Bax, activated PARP and caspase-3/9, while downregulates the level of Bcl-2. 1,3,5-Tricaffeoylquinic acid inhibits tube formation and shows cytotoxicity against ovarian cancer cells. 1,3,5-Tricaffeoylquinic acid can be used in studies related to ovarian cancer.

For research use only. We do not sell to patients.

1,3,5-Tricaffeoylquinic acid

1,3,5-Tricaffeoylquinic acid Chemical Structure

CAS No. : 1073897-80-9

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Description

1,3,5-Tricaffeoylquinic acid acts as an angiogenesis inhibitor and apoptosis inducer, and exhibits anti-HIV activity. 1,3,5-Tricaffeoylquinic acid inhibits the phosphorylation of VEGFR2, ERK, PI3K, Akt and mTOR in the angiogenesis signaling pathway. 1,3,5-Tricaffeoylquinic acid regulates apoptosis-related proteins, upregulates the levels of activated caspase-8, Bax, activated PARP and caspase-3/9, while downregulates the level of Bcl-2. 1,3,5-Tricaffeoylquinic acid inhibits tube formation and shows cytotoxicity against ovarian cancer cells. 1,3,5-Tricaffeoylquinic acid can be used in studies related to ovarian cancer[1][2].

IC50 & Target

Caspase-8

 

Caspase 3

 

Caspase-9

 

In Vitro

1,3,5-Tricaffeoylquinic acid (6.2-100 μM; 24 h) potently induces cytotoxicity in human ovarian cancer cell line A2780[1].
1,3,5-Tricaffeoylquinic acid (50-100 μM; 24 h) induces apoptotic cell death in the human ovarian cancer cell line A2780[1].
1,3,5-Tricaffeoylquinic acid (50-100 μM; 24 h) activates both exogenous and endogenous apoptotic signaling pathways in human ovarian cancer cell line A2780 after treatment at 50 and 100 μM for 24 h, upregulating pro-apoptotic proteins and downregulating the anti-apoptotic protein Bcl-2[1].
1,3,5-Tricaffeoylquinic acid (50-100 μM; 24 h) inhibits angiogenesis in HUVECs by suppressing the phosphorylation of VEGFR2 and its downstream ERK and PI3K/Akt/mTOR signaling pathways[1].
1,3,5-Tricaffeoylquinic acid (25-100 μM; 24 h) non-toxically inhibits tube formation in HUVECs, reducing tube formation by 61.77% after 24 h of treatment at 100 μM[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Viability Assay[1]

Cell Line: A2780 human ovarian cancer cells
Concentration: 6.2-100 μM
Incubation Time: 24 h
Result: Reduced cell viability to 25.81% at 100 μM.
Exhibited a concentration-dependent cytotoxic effect.
Had an IC50 of 47.43 μM.

Apoptosis Analysis[1]

Cell Line: A2780 human ovarian cancer cells
Concentration: 50-100 μM
Incubation Time: 24 h
Result: Increased the percentage of annexin V-positive apoptotic cells to 15.63% at 50 μM and 37.81% at 100 μM.

Western Blot Analysis[1]

Cell Line: HUVECs (human umbilical vein endothelial cells)
Concentration: 50-100 μM
Incubation Time: 24 h
Result: Decreased phosphorylation of VEGFR2, ERK, PI3K, Akt, and mTOR.
Enhanced these effects when co-treated with pathway inhibitors.
Increased protein expression levels of cleaved caspase-8, Bax, cleaved caspase-9, cleaved caspase-3, and cleaved PARP.
Decreased protein expression levels of Bcl-2.
Molecular Weight

678.59

Formula

C34H30O15

CAS No.
SMILES

OC1=C(O)C=CC(/C=C/C(O[C@@]2(C[C@H]([C@H](O)[C@H](OC(/C=C/C3=CC(O)=C(O)C=C3)=O)C2)OC(/C=C/C4=CC(O)=C(O)C=C4)=O)C(O)=O)=O)=C1

Structure Classification
Initial Source
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Room temperature in continental US; may vary elsewhere.

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Please store the product under the recommended conditions in the Certificate of Analysis.

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1,3,5-Tricaffeoylquinic acid
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